The metabolic balance of chicken embryos and neonatal animals can be radically altered by infection with certain viruses which contain structural lipid. This virus-induced metabolic imbalance is reflected by striking hyperlipidemias which are qualitatively and quantitatively specific for the individual viral infection. The objective of our research is to define the metabolic nature of the imbalance(s) by comparing enzymic activities, regulation of enzymic activities, and steady-state levels of intermediary metabolites in virus-infected and control embryos. These metabolic alterations will be correlated with changes in cell ultrastructure, especially those associated with membranes. Since the hyperlipidemias are the most striking signs of most of these infections, our investigations will focus on lipid metabolism and the integration of carbohydrate and lipid metabolism in this model developmental system. Hyperlipidemias occur in several different diseases and appear to predispose to others, including those of the heart and blood vessels. From our studies we hope to construct a comprehensive scheme of deranged metabolic pathways which contribute to these hyperlipidemias of known etiology and to learn the mode(s) of viral-induced alterations of host lipid metabolism which may contribute to viral pathology.